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R.: Die Therapie des chronischen Cor pulmonale. Forum cardiologicum8, 118 (1965).\nAviado, D. M.: The lung circulation. London: Pergamon Press 1965.\nBethge, J., u.H. Herzer: Die endobronchiale Streptokinase-Streptodornase-Behandlung. Bruns Beitr. Klin. Chir.192, 487 (1956).\nBopp, K. Ph., K.-J. Manns u.G. Dörner: Therapeutische Empfehlungen bei chronischen unspezifischen Erkrankungen des Respirationstraktes. Med. Klinik60, 190 (1965).\nBucher, N., u.W. Hadorn: Chronische Bronchitis. Med. Klinik55, 688 (1960).\nComroe, J. H., R. E. Forster, A. B. Dubois, W. H. Briscoe u.E. Carlsen: Die Lunge. Stuttgart: Schattauer 1964.\nDavis, A. L.: Treatment of chronic bronchitis. Amer. J. Med.31, 365 (1961).\nFerrer, J. M., R. M. Harvey, R. T. Cathcart, C. A. Webster, D. W. Richards, andA. Cournand: Some effects of digoxin upon the heart and circulation in man. Circulation1, 161 (1950).\nGordonoff, T.: Über den Standort der Expectorantien. Therap. Umschau12, 13 (1965).\nGünther, W.: Zur Behandlung der chronischen Bronchitis mit einem Streptokinase-Streptodornase-Präparat. Helv. med. acta27, 766 (1960).\n—— Die Behandlung des chronischen Cor pulmonale. Arzneitherapie2, 61 (1963).\n—— Atemmechanische Untersuchungen mit Bisolvon. Therap. Umschau12, 91 (1965).\nHamm, J., u.H. Fabel: Atemarbeit und Broncholyse bei chronischem Asthma bronchiale. Dtsch. med. Wschr.86, 2285 (1961).\n—— u.H. Fabel: Vergleichende Untersuchungen der Atemmechanik bei normaler Lungenfunktion, obstruktiven und restriktiven Ventilationsstörungen. Z. klin. Med.157, 133 (1962).\n—— Expectorantien in der Therapie von Lungenerkrankungen. Therap. Umschau12, 106 (1965).\nHarvey, R. M., M. J. Ferrer, andA. Cournand: The treatment of chronic cor pulmonale. Circulation7, 932 (1953).\nHerzog, H.: Langzeittherapie unspezifischer chronischer Lungenerkrankungen. Schweiz. med. Wschr.95, 571 (1965).\nHickam, J. B.: InCecil-Loeb: Textbook of medicine. Philadelphia: Saunders 1963.\nLyons, H. A., W. H. Becker u.G. E. Torres: Die Behandlung der schweren Formen des Lungenemphysems. Amer. J. Med.36, 62 (1964).\nMarx, H. H.: Lungenemphysem und Bronchitis. Stuttgart: Thieme 1963.\nMichel, C. F.: Blutgasuntersuchungen mit Bisolvon. Therap. Umschau12, 106 (1965).\nMargan, E., T. N. Filey, G. L. Huber, andH. Fialkow: Alterations in pulmonary surface active lipids during exposure to increased oxygen tension. J. clin. Invest.44, 1737 (1965).\nNicolas, R.: Sputumbefunde bei chronischer Bronchitis. Therap. Umschau12, 103 (1965).\nNoehren, T. H.: Pulmonary emphysema. J. Amer. med. Ass.182, 889 (1962).\nSchmidt, O. P., W. Günther u.H. Bottke: Das bronchitische Syndrom. München: Lehmann 1965.\nSoderholm, B.: Proc. First Intern. Pharmacol. Meeting (Stockholm). Pergamon Press9, 111 (1963).\nVenrath, H.: Zur Pathophysiologie der chronischen Bronchitis und des Lungenemphysems. Beitr. Klin. Tuberk.133, 203 (1966).\nVogt-Moykopf, J., u.H. Laqua: Die endobronchiale Instillation eines Bronchospasmolytikums zur Lösung von Spasmen während der Bronchographie. Thoraxchir.11, 482 (1964).\nWitek, A.: Expectorantien in der Therapie von Lungenerkrankungen. Therap. Umschau12, 106 (1965).\nZimmermann, W. E., u.H. Fischermann: Kritische Beurteilung der Behandlungsergebnisse des Bronchialcarcinoms. Med. Klinik59, 507 (1964).\nZöllner, N., G. Parrisius u.G. Linzenmeier: Langzeittherapie der chronischen Bronchitis mit Tetracyclinen. Dtsch. med. Wschr.88, 1457 (1963).",{"EN":651},"Bei der Behandlung der chronischen Bronchitis steht die Beseitigung der obstruktiven Ventilationsstörung im Vordergrund. Durch Antibiotica und Chemotherapeutica, eventuell in Form einer Langzeittherapie, kann die entzündliche Exsudation und Schwellung der Bronchialschleimhaut günstig beeinflußt werden. Unspezifische und spezifische Desensibilisierung spielen heute in der Behandlung der chronischen Bronchitis nur noch eine geringere Rolle. Zur Therapie der bronchiolären Obstruktion durch Schleimhautschwellung und Bronchospasmus stehen verschiedene Substanzen (Sympathicomimetica, Purinkörper, Anticholinergica, Hypophysenhinterlappenextrakte) zur Verfügung. Ihre Anwendung in ausreichender Dosierung ist in jedem Fall indiziert. Ein indirekter bronchospasmolytischer Effekt kommt auch den Corticosteroiden und dem ACTH durch ihre antiphlogistische und antiallergische Wirkung zu. In mittlerer Dosierung ist der Erfolg dieser Therapie bei der chronischen Bronchitis häufig gut. Ist die bronchioläre Obstruktion durch eine Sekretverlegung der Bronchioli bedingt, sind Expektorantien, bei denen Secretomotorica und Secretolytica unterschieden werden können, angezeigt. Ziel der Behandlung des Lungenemphysems ist die Vermeidung von Komplikationen durch Infektionen, Herzbelastung und Auftreten einer manifesten respiratorischen Insuffizienz. Zahlreiche Substanzen führen zwar zu einer Senkung des Pulmonalarteriendruckes, haben sich aber in der Klinik mit Ausnahme der Rauwolfia-Alkaloide wegen der zum Teil großen Nebenwirkungen und kurzen Wirkungsdauer nicht durchgesetzt. Bei der Digitalisbehandlung des Cor pulmonale ist zwischen der initialen Kompensations- und Erhaltungsbehandlung zu unterscheiden. Wegen der unsicheren Resorptionsverhältnisse durch Leberstauung und Stauungsgastritis ist bei der initialen Kompensationsbehandlung der parenteralen Strophanthin- oder Digitoxin-Therapie der Vorrang zu geben. Für die orale Langzeittherapie haben sich Präparate aus der Digoxingruppe mit mittlerer Haftfestigkeit vielfach bewährt. Eine wünschenswerte Steigerung der alveolären Ventilation kann durch zentralangreifende Substanzen erzielt werden. Jedoch sind im allgemeinen die erforderlichen Dosen recht hoch bei gleichzeitig kurzer Wirkungsdauer. Der Carboanhydrasehemmer Diamox führt hingegen über eine metabolische Acidose zu einer Anregung des Atemzentrums mit gesteigerter alveolärer Ventilation. In schweren Fällen kommt der mechanischen Beatmung, z.B. mit dem druckgesteuerten Bird-Respirator, heute eine große Bedeutung zu. Eine Sauerstoff-Therapie sollte beim Emphysematiker nur bei gleichzeitiger Beatmung oder medikamentöser Anregung des Atemzentrums vorgenommen werden.",{"EN":653},"Therapie der Bronchitis und des Emphysems",{"VOID":655},"10.1007\u002FBF02116600","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF02116600",[658],{"id":659,"sortIndex":21,"researcher":20,"roles":660,"affiliations":661,"properties":670},"fbdd23bc-3674-4f7a-bd5d-db76c89b6861",[351],[662],{"id":20,"sortIndex":21,"affiliation":663,"properties":20},{"id":664,"createTime":665,"updateTime":665,"relativeEntities":666,"slug":20,"properties":667,"entityType":40,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"50c370bc-a91d-4594-b6fa-d7a15701aab4","2024-01-20T23:58:47.891+00:00",[],{"title":668},{"VI":669},"Medizinische Klinik der Westfälischen Wilhelms-Universität Münster, Germany",{"title":671},{"VI":672},"Everhard 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Thorax 32:45–52\nCotes JE (1979) Lung function throughout life; determinants and reference values. In: Cotes JE (ed) Lung function assessment and application in medicine, 4th edn. Blackwell, London, pp 329–387\nCoutts LL, Turner-Warwick M (1982) Factors predicting outcome in intrapulrnonary fibrosis associated with asbestos exposure (asbestosis). International Conference on Occupational Lung Diseases, Chicago 1982\nCraighead JE, Abraham JL, Churg A, Green FHY, Kleinerman J, Pratt PhC, Seemayer TA, Vallyathan V, Weill H (1982) The pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Arch Pathol Lab Med 105:544–594\nFinkelstein MM (1982) Asbestosis in long-term employees of an Ontario asbestos-cement factory. Am Rev Respir Dis 125:496–501\nFournier-Massey G, Becklake MR (1975) Pulmonary function profiles in Quebec asbestos workers. 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Bei 17 Arbeitern wurde ein Lungenoedem manifest, 7 Patienten sind innerhalb weniger Stunden verstorben. Bei einzelnen Überlebenden wechselten innerhalb der ersten Tage nach dem Unglück scheinbare Besserungen mit lebensbedrohenden Situationen ab. Empfehlungen zur Behandlung des toxischen Lungenoedems werden gegeben. Es wird darauf verwiesen, daß im Anschluß an die Inhalation von Nitrosegasen ein Lungenoedem auch nach Intervallen von Stunden bis Tagen auftreten kann. Der Entstehungsmechanismus wird diskutiert. 13 Versehrte wurden 1967 begutachtet. Sieben Jahre nach dem Unglück konnten von 27 Überlebenden 24 einer Kontrolluntersuchung unterzogen werden. Es handelte sich um 18 Chemiearbeiter und sechs Bauarbeiter, die zum Zeitpunkt des Unglücks mit Montagearbeiten in dem Chemiebetrieb beschäftigt waren. Klinische Daten und Ergebnisse der Lungenfunktionsprüfung werden detailliert angeführt. Die wichtigsten Resultate sind: bei den 10 Personen, die ein Lungenoedem durchgemacht hatten, ist sieben Jahre nach dem Unglück C dyn gegenüber dem Normwert deutlich erniedrigt, dies wird als Elastizitätseinbuße interpretiert. Gegenüber 1967 ist allerdings eine Besserung erkennbar. 1967 betrug der Mittelwert für C dyn 103 ml\u002Fcm H2O, 1973 124 ml\u002Fcm H2O (Normwert größer als 200), der Unterschied ist statistisch signifikant. 1967 lag die Resistence bei 1,9 cm H2O\u002Fl\u002Fsec, 1973 bei 4,6 cm H2O\u002Fl\u002Fsec (Norm kleiner als 3,0 cm H2O\u002Fl\u002Fsec). Bei acht Chemie-und fünf Bauarbeitern war der Vergleich der Resistance zwischen 1967 und 1973 möglich. Bei den Chemiearbeitern lauten die Mittelwerte: 2,1 cm H2O\u002Fl\u002Fsec, bzw. 6,0 cm H2O\u002Fl\u002Fsec. Bei den Bauarbeitern: 1,7 cm H2O\u002Fl\u002Fsec, bzw. 2,6 cm H2O\u002Fl\u002Fsec. 1967 war bei keinem der 18 Chemiearbeiter die Resistance größer als 3,0. 1973 überschritten sieben diesen Wert. Bei den Bauarbeitern lagen 1967 ebenfalls alle Resistencewerte unter 3,0. 1973 war nur ein Wert höher. Als mögliche Ursache für diese unterschiedliche Entwicklung der Resistance bei den Chemie-und Bauarbeitern, die in Hinblick auf das Lebensalter keinen signifikanten Unterschied aufwiesen, wird die im Chemiebetrieb auch unter guten Arbeitsplatzbedingungen vorhandene Nitrosegas-Exposition diskutiert. Anhand einer reichhaltigen Literatur wird das derzeitige Wissen über den Anteil der Nitrosegase an den kumulativen Schäden, die für die Entstehung von chronischen Atemleiden verantwortlich sind, behandelt.",{"EN":966},"Wirkungen von Nitrosegasen auf die Lunge",{"VOID":968},"10.1007\u002FBF02179308","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF02179308",[971,997],{"id":972,"sortIndex":21,"researcher":20,"roles":973,"affiliations":974,"properties":994},"bda7cb43-2b04-42ca-bb6e-34a4ca188951",[351],[975,985],{"id":976,"sortIndex":181,"affiliation":977,"properties":984},"a6671547-87ae-447e-af27-dbbe52df095b",{"id":978,"createTime":979,"updateTime":979,"relativeEntities":980,"slug":20,"properties":981,"entityType":40,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"b10dcae9-266b-41ac-82a9-47ca56bfe8e2","2024-01-30T09:35:57.882+00:00",[],{"title":982},{"VI":983},"Chefärztliche Station der Allgemeinen Unfallversicherungsanstalt, Austria",{},{"id":20,"sortIndex":21,"affiliation":986,"properties":20},{"id":987,"createTime":988,"updateTime":988,"relativeEntities":989,"slug":990,"properties":991,"entityType":40,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"4f93746b-d300-4ff0-8c89-a6acb7b1f0f1","2024-04-16T21:16:58.228+00:00",[],"II-Chirurgische-Universit%C3%A4tsklinik-Wien-Austria",{"title":992},{"EN":993},"II. 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Am J Respir Crit Care Med 178:1055–1059\nKlings E, Wyszynski DF, Nolan VG, Steinberg MH (2006) Abnormal pulmonary function in adults with sickle cell anemia. Am J Respir Crit Care Med 173:1264–1269\nNational Heart, Lung, and Blood Institute (2009) About sickle cell disease. Retrieved from http:\u002F\u002Fwww.nhlbi.nih.gov\u002Fmeetings\u002Fworkshops\u002FSickle_Cell_Disease_Workshop.pdf\nPlatt OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, Klug PP (1994) Mortality of sickle cell disease – life expectancy and risk factors for early death. N Engl J Med 330:1639–1644\nCaboot JB, Allen JL (2008) Pulmonary complications of sickle cell disease in children. Curr Opin Pediatr 20:279–287\nField JJ, Glassberg J, Gilmore A et al (2008) Longitudinal analysis of pulmonary function in adults with sickle cell disease. Am J Hematol 83:574–576\nShirlo NR, Lands LC (2011) Asthma and sickle cell chronic lung disease: a dynamic relationship. Peadiatr Respir Review 12:78–82\nYoung RC, Castro O, Baxter R et al (1981) The lung in sickle cell disease: a clinical overview of common vascular, infectious, and other problems. J National Med Assoc 73(1):19–26\nSiddiqui AK, Ahmed S (2003) Pulmonary manifestations of sickle cell disease. Postgrad Med J 79:384–390\nVij R, Machado RF (2010) Pulmonary complications of hemoglobinopathies. Chest 138(4):973–983\nYoung RC, Wright P, Banks DD (1976) Lung function abnormalities occurring in sickle cell hemoglobinopathies – a preliminary report. J National Med Assoc 68(3):201–205\nPianosi P, D’Souza SJ, Charge TD, Esseltine DE, Coates A (1993) Pulmonary function abnormalities in childhood sickle cell disease. J Pediatr 122:366–371\nMiller GJ, Serjeant GR (1971) An assessment of lung volumes and gas transfer in sickle-cell anaemia. Thorax 26:309–315\nMiller GJ, Serjeant GR, Saunders MJ, Richardson C, Gilson RJC (1978) Interpretation of lung function tests in the sickle-cell haemoglobinopathies. Thorax 33:85–88\nSylvester KP, Patey RA, Milligan P et al (2004) Pulmonary function abnormalities in children with sickle cell disease. Thorax 59:67–70\nFemi-Pearse D, Gazioglu KM, Yu PN (1970) Pulmonary function studies in sickle cell disease. J Appl Physiol 28:574–577\nAmerican Thoracic Society (1991) Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis 144:1202–1218\nAmerican Thoracic Society (1991) Standardization of spirometry: 1994 update. Am Rev Respir Dis 144:1202–1218\nBoyd JH, DeBaun MR, Morgan WJ, Mao J, Strunk RC (2009) Lower airway obstruction is associated with increased morbidity in children with sickle cell disease. Pediatr Pulmonol 44(3):290–300\nZapletal A, Samanek M, Paul T (1987) Lung function in children and adolescents: methods, reference values. 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Pediatr Pulmonol 42:103–106\nField JJ, DeBaun MR (2009) Asthma and sickle cell disease: two distinct diseases or part of the same process. Hematology Am Soc Hematol Educ Program 1:45–53\nMorris C (2009) Asthma management: reinventing the wheel in sickle cell disease. Am J Hematol 84:234–241\nSchroeder SA, Nepo AG (2008) Treatment of asthma in children with sickle cell disease can prevent recurrences of acute chest syndrome. Am J Respir Crit Care Med 177:A262\nIntzes S, Kalpatthi RV, Short R, Imran H (2013) Pulmonary function abnormalities and asthma are prevalent in children with sickle cell disease and are associated with acute chest syndrome. Pediatr Hematol Oncol 27:1–7\nRhodes M, Akohoue S, Shankar S et al (2009) Growth patterns in children with sickle cell anemia during puberty. Pediatr Blood Cancer 53(4):635–641\nSinghal A, Thomas P, Cook R, Wierenga K, Serjeant G (1994) Delayed adolescent growth in homozygous sickle cell disease. Arch Dis Childhood 71:404–408\nPhebus CK, Gloninger MF, Maciak BJ (1984) Growth patterns by age and sex in children with sickle cell disease. J Pediatr 105(1):28–33\nKoumbourlis AC, Lee DJ, Lee A (2007) Longitudinal changes in lung function and somatic growth in children with sickle cell disease. Pediatr Pulmonol 42:483–488\nMcCormack MK, Dicker L, Katz SH et al (1976) Growth patterns of children with sickle cell disease. Human Biol 48(3):429–437\nKoumbourlis AC, Hurlet-Jensen A, Bye MR (1997) Lung function in infants with sickle cell disease. Pediatr Pulmonol 24:277–281\nKoumbourlis AC, Zar H, Hurlet-Jensen A, Goldberg M (2001) Prevalence and reversibility of lower airway obstruction in children with sickle cell disease. J Pediatr 138:188–192\nTassel C, Arnaud C, Kulpa M et al (2011) Leukocytosis is a risk factor for lung deterioration in children with sickle cell disease. Respir Med 105(5):788–795",{"EN":1060},"The\n pulmonary complications of sickle cell disease (SCD) are a leading cause of morbidity and mortality (MacLean et al. Am J Respir Crit Care Med 178:1055–1059, 2008; Klings et al. Am J Respir Crit Care Med 173:1264–1269, 2006; National Heart, Lung, and Blood Institute, 2009). Despite this recognition, predictive markers of lung dysfunction progression remain elusive (Klings et al. Am J Respir Crit Care Med 173:1264–1269, 2006; Platt et al. N Engl J Med 330:1639–1644, 1994; Caboot et al. Curr Opin Pediatr 20:279–287, 2008; Field et al. Am J Hematol 83:574–576, 2008; Shirlo et al. Peadiatr Respir Review 12:78–82, 2011). This study was designed describe the longitudinal progression and identify specific markers that influence bronchial disease in SCD. A retrospective, chart review of 89 patients with SCD was conducted. All patients underwent spirometry in conjunction with body plethysmography as part of routine care. Eleven lung function variables were assessed, five of which were selected to establish patterns of normal, obstructive, restrictive, or mixed obstructive-restrictive physiology (Klings et al. Am J Respir Crit Care Med 173:1264–1269, 2006; Field et al. Am J Hematol 83:574–576, 2008). In the unadjusted model, forced expiratory volume in one second (FEV1)% of predicted trended downward with age, while total lung capacity (TLC)% of predicted showed a bimodal distribution and carbon monoxide diffusion capacity corrected for hemoglobin (DLCOcor)% of predicted remained stable. Adjusting for acute chest syndrome (ACS) episodes, medication status, and growth velocity (GV), the final model demonstrated that the downward trend between FEV1% of predicted with age was further influenced by the latter two factors. Initial decline in FEV1% of predicted is associated with worsening pulmonary dysfunction over time. Independent of ACS episodes, the factors most influential on the progression of FEV1% predicted include the introduction of medications as well as the promotion of adequate prepubertal growth. Efforts to ensure normal prepubertal GV and treatment with bronchodilators, such as short-acting beta2 agonists and inhaled corticosteroids (ICS), should be considered at an early age to delay progression of pulmonary dysfunction.",{"EN":1062},"Progression and Prognostic Indicators of Bronchial Disease in Children with Sickle Cell Disease",{"VOID":1064},"10.1007\u002Fs00408-014-9572-y","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00408-014-9572-y",[1067,1094,1118,1138,1158],{"id":1068,"sortIndex":21,"researcher":20,"roles":1069,"affiliations":1070,"properties":1091},"b1bc8e77-7769-47e1-b9da-9641373982a0",[351],[1071,1079],{"id":20,"sortIndex":21,"affiliation":1072,"properties":20},{"id":1073,"createTime":1074,"updateTime":1074,"relativeEntities":1075,"slug":20,"properties":1076,"entityType":40,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"c622b5a5-d982-4ec5-a32e-7613064f81da","2023-12-29T23:57:57.852+00:00",[],{"title":1077},{"VI":1078},"Pediatric Pulmonology\u002FAllergy\u002FImmunology, Miller Children’s Hospital, Long Beach, USA",{"id":1080,"sortIndex":181,"affiliation":1081,"properties":1090},"d3d3232d-a77a-4e93-acb3-bef67bd33940",{"id":1082,"createTime":1083,"updateTime":1084,"relativeEntities":1085,"slug":1086,"properties":1087,"entityType":40,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"28db5e5e-43db-45c4-80f3-c64cf5976830","2024-01-09T23:04:15.598+00:00","2024-09-12T15:26:24.931+00:00",[],"University-of-California-Irvine-USA",{"title":1088},{"VI":1089},"University of California-Irvine, USA",{},{"title":1092},{"VI":1093},"Sophia N. 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